Thomas Hamilton to Speak About the Cytokine Regulation at Cytokines Conf., Jan. 29-31, 2014, SD, CA
Thomas Hamilton, Chairman of the Department of Immunology at the Lerner Research Institute at the Cleveland Clinic, Will Speak About "Regulation of TLR-Induced Cytokine Expression by Environmental Stress" at the 12th Cytokines & Inflammation Conference, January 29-31, 2014 in San Diego, CA.
- (1888PressRelease) October 08, 2013 - Thomas Hamilton will present about "Regulation of TLR-Induced Cytokine Expression by Environmental Stress" at the 12th Cytokines & Inflammation Conference, to be held January 29-31, 2014 in San Diego, CA.
Dr. Hamilton currently serves as the Chairman of the Department of Immunology at the Lerner Research Institute of the Cleveland Clinic Foundation, where his research focuses on studying the regulation of inflammatory cytokine and chemokine gene expression. His laboratory has made substantial contributions to the understanding of both transcriptional and post-transcriptional control mechanisms regulating innate inflammatory responses in myeloid and non-myeloid cell populations.
He will discuss how cellular stress can amplify the expression of selected inflammatory cytokines in myeloid cell populations. For example, TLR-stimulated CXCL1 and CXCL2 chemokine mRNA levels are enhanced more than ten-fold in stressed macrophages, while mRNAs encoding CCL5 and CXCL10 are not. Other pro-inflammatory cytokines that show elevated levels of stress include TNFa, IL-1a, and IL-6.
Stress responses also enhance chemokine protein levels during peritoneal inflammation. TLR4 is the most sensitive, though other TLR responses are also enhanced. Stress-enhanced chemokine gene expression is mediated by altered transcription, but NFkB activation, though necessary, does not appear to be the target of stress.
Similarly, while the IRF3 transcription factor is linked to TLR4 signaling, IRF3 is not required for stress sensitivity. Though mediators of endoplasmic reticulum stress (IRE-1, XBP-1, and CHOP) have been implicated in altered inflammatory cytokine responses, they are not required for amplification of TLR4-induced chemokine expression. Rather, RIP1, a kinase that participates in TLR3 andTLR4/TRIF signaling, is required through a pathway that involves stress-dependent increases in RIP1 protein levels and activation via ubiquitinylation.
Dr. Hamilton will discuss how these findings, which identify novel mechanisms for modulating the magnitude and duration of selective TLR-induced chemokine and cytokine gene expression, further establish the importance of environmental stress in coordinating the outcomes of cellular and tissue injury.
For more information, please visit www.gtcbio.com/cyto.
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